These studies indicate that loss of a classic tumor suppressor, like the TP53 gene, is a main factor that releases the brake and allows cell populations with CIN to keep proliferating (Sansregret et al. 2018), suggesting this mechanism may be linked to a DNA damage response triggered by chromosome missegragations that induce breaks in the DNA. Here, TP53 is linked to cervical squamous intraepithelial neoplasia.